The symptoms of Dysautonomia, which are numerous and vary widely for each individual, are due to inefficient or unbalanced efferent signals sent via both systems. The primary symptoms in individuals with dysautonomia include

Dysautonomia may be due to inherited or degenerative neurologic diseases (primary dysautonomia) or it may occur due to injury of the autonomic nervous system from an acquired disorder (secondary dysautonomia). The most common causes of dysautonomia include

In the sympathetic nervous system (SNS), predominant dysautonomia is common along with fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, and interstitial cystitis, raising the possibility that such dysautonomia could be their common clustering underlying pathogenesis.

In addition to sometimes being a symptom of dysautonomia, anxiety can sometimes physically manifest symptoms resembling autonomic dysfunction. A thorough investigation ruling out physiological causes is crucial, but in cases where relevant tests are performed and no causes are found or symptoms do not match any known disorders, a primary anxiety disorder is possible, but should not be presumed. For such patients, the anxiety sensitivity index may have better predictivity for anxiety disorders, while the Beck anxiety inventory may misleadingly suggest anxiety for patients with dysautonomia.

Primary autonomic failure (also called primary dysautonomia) refers to a category of dysautonomias -- conditions in which the autonomic nervous system does not function properly.

In primary dysautonomias, the autonomic dysfunction occurs as a primary condition (as opposed to resulting from another disease). Autonomic failure is categorized as "primary" when believed to result from a chronic condition characterized by degeneration of the autonomic nervous system, or where autonomic failure is the predominant symptom and its cause is unknown.

Such "primary" dysautonomias are distinguished from secondary dysautonomias, where the dysfunction of the autonomic nervous system is believed to be caused by another disease (e.g. diabetes).

Diseases categorized as primary autonomic failure usually include pure autonomic failure and multiple system atrophy. Many scientists also categorize Parkinson disease and familial dysautonomia as "primary".

A degenerative disease of the autonomic nervous system, symptoms include dizziness and fainting (caused by orthostatic hypotension), visual disturbances and neck pain. Chest pain, fatigue and sexual dysfunction are less common symptoms that may also occur. Symptoms are worse when standing; sometimes one may relieve symptoms by lying down.

The signs and symptoms of autonomic neuropathy include the following:

- Urinary bladder conditions: bladder incontinence or urinary retention

- Gastrointestinal tract: dysphagia, abdominal pain, nausea, vomiting, malabsorption, fecal incontinence, gastroparesis, diarrhoea, constipation

- Cardiovascular system: disturbances of heart rate (tachycardia, bradycardia), orthostatic hypotension, inadequate increase of heart rate on exertion

- Respiratory system: impairments in the signals associated with regulation of breathing and gas exchange (central sleep apnea, hypopnea, bradypnea).

- Nervous system: pupillary defect, exaggerated hippus, dizziness or lightheadedness.

- Other areas: hypoglycemia unawareness, genital impotence, sweat disturbances, sicca (dryness).

The pathology of pure autonomic failure is not yet completely understood. However, a loss of cells in the intermediolateral column of the spinal cord has been documented, as has a loss of catecholamine uptake and catecholamine fluorescence in sympathetic postganglionic neurons. In general, levels of catecholamines in these patients are very low while lying down, and do not increase much upon standing.

Although symptoms of AAG can range from patient to patient, hallmark symptoms include:

- gastrointestinal dysmotility

- anhidrosis (decreased ability to sweat)

- bladder dysfunction (neurogenic bladder)

- small fiber peripheral neuropathy

- Severe orthostatic hypotension

- Pupillary dysfunction

- syncope (fainting)

- Sicca syndrome (chronic dryness of the eyes and mouth)

Autonomic neuropathy (also AN or AAN) is a form of polyneuropathy that affects the non-voluntary, non-sensory nervous system (i.e., the autonomic nervous system), affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen, and pelvis outside the spinal cord. They have connections with the spinal cord and ultimately the brain, however. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In most—but not all—cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.

Autonomic neuropathy is one cause of malfunction of the autonomic nervous system (referred to as dysautonomia), but not the only one; some conditions affecting the brain or spinal cord also may cause autonomic dysfunction, such as multiple system atrophy, and therefore, may cause similar symptoms to autonomic neuropathy.

The most distinctive clinical feature is the absence of overflow tears with emotional crying after age 7 months. This symptom can manifest less dramatically as persistent bilateral eye irritation. There is also a high prevalence of breech presentation. Other symptoms include weak or absent suck and poor tone, poor suck and misdirected swallowing, and red blotching of skin.

Symptoms in an older child with familial dysautonomia might include:

1. Delayed speech and walking

2. Unsteady gait

3. Spinal curvature

4. Corneal abrasion

5. Less perception in pain or temperature with nervous system.

6. Poor growth

7. Erratic or unstable blood pressure.

8. Red puffy hands

9. Dysautonomia crisis: a constellation of symptoms in response to physical and emotional stress; usually accompanied by vomiting, increased heart rate, increase in blood pressure, sweating, drooling, blotching of the skin and a negative change in personality.

Familial dysautonomia (FD), sometimes called Riley–Day syndrome and hereditary sensory and autonomic neuropathy type III (HSAN-III), is a disorder of the autonomic nervous system which affects the development and survival of sensory, sympathetic and some parasympathetic neurons in the autonomic and sensory nervous system resulting in variable symptoms, including insensitivity to pain, inability to produce tears, poor growth, and labile blood pressure (episodic hypertension and postural hypotension). People with FD have frequent vomiting crises, pneumonia, problems with speech and movement, difficulty swallowing, inappropriate perception of heat, pain, and taste, as well as unstable blood pressure and gastrointestinal dysmotility. FD does not affect intelligence. Originally reported by Drs. Conrad Milton Riley (1913–2005) and Richard Lawrence Day (1905–1989) in 1949, FD is one example of a group of disorders known as hereditary sensory and autonomic neuropathies (HSAN). All HSAN are characterized by widespread sensory dysfunction and variable autonomic dysfunction caused by incomplete development of sensory and autonomic neurons. The disorders are believed to be genetically distinct from each other.

Autoimmune autonomic ganglionopathy (AAG) is an extremely rare form of dysautonomia in which the patients immune system produces ganglionic AChR antibodies, inhibiting ganglionic AChR currents and impairing transmission in autonomic ganglia. Approximately 100 Americans are diagnosed with AAG each year. Symptoms onset can be acute, subacute or gradual.

Patients who suffer from acute OI usually manifest the disorder by a temporary loss of consciousness and posture, with rapid recovery (simple faints, or syncope), as well as remaining conscious during their loss of posture. This is different from a syncope caused by cardiac problems because there are known triggers for the fainting spell (standing, heat, emotion) and identifiable prodromal symptoms (nausea, blurred vision, headache). As Dr. Julian M. Stewart, an expert in OI from New York Medical College states, "Many syncopal patients have no intercurrent illness; between faints, they are well."

Symptoms:

- Altered vision (blurred vision, "white outs"/gray outs, black outs, double vision)

- Anxiety

- Exercise intolerance

- Fatigue

- Headache

- Heart palpitations, as the heart races to compensate for the falling blood pressure

- Hyperpnea or sensation of difficulty breathing or swallowing (see also hyperventilation syndrome)

- Lightheadedness

- Sweating

- Tremulousness

- Weakness

A classic manifestation of acute OI is a soldier who faints after standing rigidly at attention for an extended period of time.

Orthostatic intolerance is divided, roughly based on patient history, in two variants: acute and chronic.

Movement Disorder

- Dystonia

- Parkinsonism

- Chorea

- Ocular flutter

- Motor tics

Psychiatric Symptoms

- Agitation

- Emotional lability

- Psychosis

- Depression

Associated symptoms

- Encephalopathy

- Sleep disorder

- Reduced consciousness

- Mutism

Five different clinical entities have been described under hereditary sensory and autonomic neuropathies – all characterized by progressive loss of function that predominantly affects the peripheral sensory nerves. Their incidence has been estimated to be about 1 in 25,000.

Age: Adult and Elderly

Sex: Both

Onset : Subacute

Behavior change

Memory loss, confabulation

Confusion and disorientation

Hallucinations

Dyssomnia

Seizures focal and generalized, myoclonic

Extrapyramidal dysfunction

Brainstem/cranial nerve dysfunction

Dysautonomia

Neuromyotonia

Peripheral nerve dysfunction

Hyponatreamia

Characteristics of paroxysmal sympathetic hyperactivity include:

- fever

- tachycardia

- hypertension

- tachypnea

- hyperhidrosis or diaphoresis

- dystonic posturing

- pupillary dilation

- flushing

In cases where PSH episodes develop post-injury, specifically traumatic brain injury, symptoms typically develop quickly, usually within a week. Symptom onset has been seen to average 5.9 days post-injury. Episodes vary in duration and occurrence. Episodes can last as little as a few minutes or as long as ten hours, and they can occur multiple times a day. Episode duration has been seen to average 30.8 minutes and occur five to six times a day. Episodes can occur naturally or arise from external triggers. Common triggers include pain or stimulation, body turning or movements, and bladder distention. Bladder distention has been observed in patients being treated in intensive care units with the concurrent use of catheters. Symptoms of PSH can last from weeks to years following initial onset. As episodes persist over time, they have been found to become less frequent in occurrence but last for prolonged periods.

Congenital insensitivity to pain with anhidrosis (CIPA), also known as hereditary sensory and autonomic neuropathy type IV (HSAN IV), is characterized by insensitivity to pain, anhidrosis (the inability to sweat), and intellectual disability. The ability to sense all pain (including visceral pain) is absent, resulting in repeated injuries including: oral self-mutilation (biting of tongue, lips, and buccal mucosa); biting of fingertips; bruising, scarring, and infection of the skin; multiple bone fractures (many of which fail to heal properly); and recurrent joint dislocations resulting in joint deformity. Sense of touch, vibration, and position are normal. Anhidrosis predisposes to recurrent febrile episodes that are often the initial manifestation of CIPA. Hypothermia in cold environments also occurs. Intellectual disability of varying degree is observed in most affected individuals; hyperactivity and emotional lability are common.

Hereditary sensory neuropathy type IV (HSN4) is a rare genetic disorder characterized by the loss of sensation (sensory loss), especially in the feet and legs and, less severely, in the hands and forearms. The sensory loss is due to abnormal functioning of small, unmyelinated nerve fibers and portions of the spinal cord that control responses to pain and temperature as well as other involuntary or automatic body processes. Sweating is almost completely absent with this disorder. Intellectual disability is usually present.

Type 4, congenital insensitivity to pain with anhidrosis (CIPA), is an autosomal recessive condition and affected infants present with episodes of hyperthermia unrelated to environmental temperature, anhidrosis and insensitivity to pain. Palmar skin is thickened and charcot joints are commonly present. NCV shows motor and sensory nerve action potentials to be normal. The histopathology of peripheral nerve biopsy reveals absent small unmyelinated fibers and mitochondria are abnormally enlarged.

Management of Hereditary sensory and autonomic neuropathy Type 4:

Treatment of manifestations: Treatment is supportive and is best provided by specialists in pediatrics, orthopedics, dentistry, ophthalmology, and dermatology. For anhidrosis: Monitoring body temperature helps to institute timely measures to prevent/manage hyperthermia or hypothermia. For insensitivity to pain: Modify as much as reasonable a child’s activities to prevent injuries. Inability to provide proper immobilization as a treatment for orthopedic injuries often delays healing; additionally, bracing and invasive orthopedic procedures increase the risk for infection. Methods used to prevent injuries to the lips, buccal mucosa, tongue, and teeth include tooth extraction, and/or filing (smoothing) of the sharp incisal edges of teeth, and/or use of a mouth guard. Skin care with moisturizers can help prevent palmar and plantar hyperkeratosis and cracking and secondary risk of infection; neurotrophic keratitis is best treated with routine care for dry eyes, prevention of corneal infection, and daily observation of the ocular surface. Interventions for behavioral, developmental, and motor delays as well as educational and social support for school-age children and adolescents are recommended.

Prevention of secondary complications: Regular dental examinations and restriction of sweets to prevent dental caries; early treatment of dental caries and periodontal disease to prevent osteomyelitis of the mandible. During and following surgical procedures, potential complications to identify and manage promptly include hyper- or hypothermia and inadequate sedation, which may trigger unexpected movement and result in secondary injuries.

Paroxysmal sympathetic hyperactivity (PSH) is a syndrome that causes episodes of increased activity of the sympathetic nervous system. Hyperactivity of the sympathetic nervous system can manifest as increased heart rate, increased respiration, increased blood pressure, diaphoresis, and hyperthermia.

Previously, this syndrome has been identified as general dysautonomia but now is considered a specific form of it. It has also been referred to as paroxysmal sympathetic instability with dystonia, or PAID, and sympathetic storm. Recently, however, studies have adopted the name paroxysmal sympathetic hyperactivity to ensure specificity. PSH is observed more in younger patients than older ones. It is also seen more commonly in men than women. There is no known reason why this is the case, although it is suspected pathophysiological links may exist. In patients surviving traumatic brain injury, the occurrence of these episodes is one in every three. PSH can also be associated with severe anoxia, subarachnoid and intracerebral hemorrhage, and hydrocephalus.

The hallmark sign of POTS is a measured increase in heart rate by at least 30 beats per minute within 10 minutes of assuming an upright position. For people aged between 12 and 19, the minimum increase for diagnosis is 40 beats per minute. This symptom is known as orthostatic (upright) tachycardia (fast heart rate). It occurs without any coinciding drop in blood pressure, as that would indicate orthostatic hypotension. It should be noted, however, that certain medications to treat POTS may cause orthostatic hypotension. It is accompanied by other features of orthostatic intolerance—symptoms which develop in an upright position and are relieved by reclining. These orthostatic symptoms include palpitations, light-headedness, chest discomfort, shortness of breath, nausea, weakness or "heaviness" in the lower legs, blurred vision and cognitive difficulties. Symptoms may be exacerbated with prolonged sitting, prolonged standing, alcohol, heat, exercise, or eating a large meal.

In up to one third of people with POTS, fainting occurs in response to postural changes or exercise. Migraine-like headaches are common, sometimes with symptoms worsening in an upright position (orthostatic headache). Some people with POTS develop acrocyanosis, or blotchy, red/blue skin upon standing, especially over the feet (indicative of blood pooling). 48% of people with POTS report chronic fatigue and 32% report sleep disturbances. Others exhibit only the cardinal symptom of orthostatic tachycardia.

POTS can co-occur in all types of Ehlers–Danlos syndrome (EDS), a hereditary connective tissue disorder marked by loose hypermobile joints prone to subluxations and dislocations, skin that exhibits moderate or greater laxity, easy bruising, and many other symptoms. A trifecta of POTS, EDS, and Mast Cell Activation Syndrome (MCAS) is becoming increasingly more common, with a genetic marker common among all three conditions. POTS is also often accompanied by vasovagal syncope, with a 25% overlap being reported. There is significant overlap between POTS and chronic fatigue syndrome, with evidence of POTS in 25–50% of CFS cases. Fatigue and reduced exercise tolerance are prominent symptoms of both conditions, and dysautonomia may underlie both conditions.

A neurological disorder is any disorder of the nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms. Examples of symptoms include paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be assessed by neurological examination, and studied and treated within the specialities of neurology and clinical neuropsychology.

Interventions for neurological disorders include preventative measures, lifestyle changes, physiotherapy or other therapy, neurorehabilitation, pain management, medication, or operations performed by neurosurgeons. The World Health Organization estimated in 2006 that neurological disorders and their sequelae (direct consequences) affect as many as one billion people worldwide, and identified health inequalities and social stigma/discrimination as major factors contributing to the associated disability and suffering.

Neurological disorders can be categorized according to the primary location affected, the primary type of dysfunction involved, or the primary type of cause. The broadest division is between central nervous system disorders and peripheral nervous system disorders. The Merck Manual lists brain, spinal cord and nerve disorders in the following overlapping categories:

- Brain:

- Brain damage according to cerebral lobe "(see also 'lower' brain areas such as basal ganglia, cerebellum, brainstem)":

- Frontal lobe damage

- Parietal lobe damage

- Temporal lobe damage

- Occipital lobe damage

- Brain dysfunction according to type:

- Aphasia (language)

- Dysgraphia (writing)

- Dysarthria (speech)

- Apraxia (patterns or sequences of movements)

- Agnosia (identifying things or people)

- Amnesia (memory)

- Spinal cord disorders (see spinal pathology, injury, inflammation)

- Peripheral neuropathy and other Peripheral nervous system disorders

- Cranial nerve disorder such as Trigeminal neuralgia

- Autonomic nervous system disorders such as dysautonomia, Multiple System Atrophy

- Seizure disorders such as epilepsy

- Movement disorders of the central and peripheral nervous system such as Parkinson's disease, Essential tremor, Amyotrophic lateral sclerosis, Tourette's Syndrome, Multiple Sclerosis and various types of Peripheral Neuropathy

- Sleep disorders such as Narcolepsy

- Migraines and other types of Headache such as Cluster Headache and Tension Headache

- Lower back and neck pain (see Back pain)

- Central neuropathy (see Neuropathic pain)

- Neuropsychiatric illnesses (diseases and/or disorders with psychiatric features associated with known nervous system injury, underdevelopment, biochemical, anatomical, or electrical malfunction, and/or disease pathology e.g. Attention deficit hyperactivity disorder, Autism, Tourette's syndrome and some cases of obsessive compulsive disorder as well as the neurobehavioral associated symptoms of degeneratives of the nervous system such as Parkinson's disease, essential tremor, Huntington's disease, Alzheimer's disease, multiple sclerosis and organic psychosis.)

Many of the diseases and disorders listed above have neurosurgical treatments available (e.g. Tourette's Syndrome, Parkinson's disease, Essential tremor and Obsessive compulsive disorder).

- Delirium and dementia such as Alzheimer's disease

- Dizziness and vertigo

- Stupor and coma

- Head injury

- Stroke (CVA, cerebrovascular attack)

- Tumors of the nervous system (e.g. cancer)

- Multiple sclerosis and other demyelinating diseases

- Infections of the brain or spinal cord (including meningitis)

- Prion diseases (a type of infectious agent)

- Complex regional pain syndrome (a chronic pain condition)

Neurological disorders in non-human animals are treated by veterinarians.

Symptoms may last for days, weeks, or months until the injury is healed. The most apparent sign of hypermetabolism is an abnormally high intake of calories followed by continuous weight loss. Internal symptoms of hypermetabolism include but are not limited to: peripheral insulin resistance, elevated catabolism of protein, carbohydrates and triglycerides, and a negative nitrogen balance in the body.

Outward symptoms of hypermetabolism may include:

- Sudden weight loss

- Anemia

- Fatigue

- Elevated heart rate

- Irregular heartbeat

- Insomnia

- Dysautonomia

- Shortness of breath

- Muscle weakness

- Excessive sweating

Dopamine beta (β)-hydroxylase deficiency is a condition that affects the autonomic nervous system (ANS). The ANS works via two opposing branches, the sympathetic and parasympathetic, both of which antagonistically control involuntary processes that regulate bodily homeostasis. Problems related to DβH deficiency often first appear as complications shortly after birth. Postnatal episodes may include vomiting, dehydration, hypotension, muscle hypotonia, hypothermia, and hypoglycemia.

Due to the deficiency of norepinephrine and epinephrine those affected by dopamine β-hydroxylase deficiency may present with droopy eyelids (ptosis), nasal congestion, and hypotension. The most common complaint of individuals with dopamine β-hydroxylase deficiency is orthostatic hypotension. The symptoms associated with orthostatic hypotension are dizziness, blurred vision, or fainting upon standing. Therefore, DβH deficiency patients may have an inability to stand for a prolonged period of time. This phenomenon is especially pronounced when going from supine to upright positions, such as getting out of bed in the morning. It is also worsened by extreme climates due to loss of fluid through excessive sweating. The inability to maintain normal blood pressure makes it difficult for people with DβH deficiency to exercise (exercise intolerance). Males with DβH deficiency may experience retrograde ejaculation, a discharge of semen backward into the bladder due to dysmotility of their smooth muscle, which as innervated by the ANS. A subset of DβH deficiency patients present with hypermobility. Postural orthostatic tachycardia syndrome, another form of dysautonomia, also sees this comorbidity with hypermobility in the form of a rare connective tissue disorder called Ehlers Danlos syndrome.

Another commonly experienced symptom is hypoglycemia, which is thought to be caused by adrenomedullary failure. In looking at the cardiovascular system, a loss of noradrenergic control is seen as T-wave abnormalities on electrocardiogram. Prolactin is frequently suppressed by excessive dopamine found in the patient's central nervous system. Excess dopamine can also affect digestion, producing vomiting and inhibiting motor signaling to the GI tract.

Many different illnesses can cause an increase in metabolic activity as the body combats illness and disease in order to heal itself.

Hypermetabolism is a common symptom of various pathologies. Some of the most prevalent diseases characterized by hypermetabolism are listed below.

- Hyperthyroidism: Manifestation: An overactive thyroid often causes a state of increased metabolic activity.

- Friedreich's ataxia: Manifestation: Local cerebral metabolic activity is increased extensively as the disease progresses.

- Fatal familial insomnia: Manifestation: Hypermetabolism in the thalamus occurs and disrupts sleep spindle formation that occurs there.

- Graves' disease: Manifestation: Excess hypermetabolically-induced thyroid hormone activates sympathetic pathways, causing the eyelids to retract and remain constantly elevated.

- Anorexia and bulimia: Manifestation: The prolonged stress put on the body as a result of these eating disorders forces the body into starvation mode. Some patients recovering from these disorders experience hypermetabolism until they resume normal diets.

- Astrocytoma: Manifestation: Causes hypermetabolic lesions in the brain